MiR-135b promotes proliferation and invasion of osteosarcoma cells via targeting FOXO1

Pei, Hong; Jin, Zhiliang; Chen, Shunguang; Sun, Xianglun; Yu, Jin; Guo, Weichun

doi:10.1007/s11010-014-2281-2

Cited by 53 publications

(42 citation statements)

References 27 publications

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“…MiRNA expression and biological function have been studied in various tumors. MiRNA microarrays have clarified their relationship with tumor occurrence, development, and differentiation, and in favor of tumor diagnosis and classification Pei et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Regulatory role of microRNA184 in osteosarcoma cells

Gr¹,

Wang²,

Xb³

et al. 2015

Genet. Mol. Res.

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Section: Discussionmentioning

confidence: 99%

Regulatory role of microRNA184 in osteosarcoma cells

Gr¹,

Wang²,

Xb³

et al. 2015

Genet. Mol. Res.

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“…[1][2][3][4][5] With the improvements of osteosarcoma therapeutic strategies including adjuvant chemotherapy, radiotherapy and wide tumour excision, the 5-year survival rate of osteosarcoma cases without metastatic disease is improved to 65%. [6][7][8][9] However, a half of patients will develop metastases and few of these patients could be cured.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of lncRNA CASC2 facilitates osteosarcoma growth and invasion through miR‐181a

Hao

et al. 2017

Cell Proliferation

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Objectives: Long non-coding RNA cancer susceptibility candidate 2 (CASC2) is a novel lncRNA and has been indicated as playing tumour suppressor gene in several tumours.However, the role of CASC2 in osteosarcoma is still uncovered. Materials and methods:The CASC2 and miR-181a expressions were measured via qRT-PCR. CCK-8 assay and colony formation assay were performed to determine the cell growth, and transwell assay was performed to assess the cell invasion. Results:We showed that CASC2 expression was downregulated in osteosarcoma samples and cell lines. Moreover, we showed that downregulated expression of CASC2 was correlated with advanced TNM stage. Furthermore, overexpression of CASC2 inhibited osteosarcoma cell proliferation, colony formation, and invasion. In addition, we indicated that ectopic expression of CASC2 suppressed miR-181a expression and enhanced the expression of Ras association domain family member 6 (RASSF6), PTEN and ATM in osteosarcoma cell, which were the direct target gene of miR-181a. Moreover, we indicated that RASSF6 expression was downregulated in osteosarcoma samples and cell lines and downregulated expression of RASSF6 was correlated with advanced TNM stage. We found that the expression of RASSF6 was positively correlated with the expression of CASC2 in osteosarcoma tissues. Ectopic expression of CASC2 suppressed the osteosarcoma cell proliferation, colony formation and invasion through regulating RASSF6 expression. Conclusions:Our data illuminated that CASC2 acted as a tumour suppressor in osteosarcoma progression.

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“…Recent studies have shown that hyperactivation of the Notch or Wnt/β-catenin pathways in tumors is partly associated with the dysregulation of certain microRNAs (miRNAs) that in turn regulate the Notch or Wnt/β-catenin pathways 23, 24. Aberrantly regulated expression of miR-135b has been detected in several types of tumors including OS 25, 26. Interestingly, although not in tumors, upregulated miR-135b results in the activation of Wnt/β-catenin signaling in glomerulopathies 27 .…”

Section: Introductionmentioning

confidence: 99%

miR-135b Stimulates Osteosarcoma Recurrence and Lung Metastasis via Notch and Wnt/β-Catenin Signaling

Jin

Luo

Wang

et al. 2017

Molecular Therapy - Nucleic Acids

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Cancer stem cells (CSCs) play an important role in osteosarcoma (OS) metastasis and recurrence, and both Wnt/β-catenin and Notch signaling are essential for the development of the biological traits of CSCs. However, the mechanism that underlies the simultaneous hyperactivation of both Wnt/β-catenin and Notch signaling in OS remains unclear. Here, we report that expression of miR-135b correlates with the overall and recurrence-free survival of OS patients, and that miR-135b has an activating effect on both Wnt/β-catenin and Notch signaling. The overexpression of miR-135b simultaneously targets multiple negative regulators of the Wnt/β-catenin and Notch signaling pathways, including glycogen synthase kinase-3 beta (GSK3β), casein kinase 1a (CK1α), and ten-eleven translocation 3 (TET3). Therefore, upregulated miR-135b promotes CSC traits, lung metastasis, and tumor recurrence in OS. Notably, antagonizing miR-135b potently inhibits OS lung metastasis, cancer cell stemness, CSC-induced tumor formation, and recurrence in xenograft animal models. These findings suggest that miR-135b mediates the constitutive activation of Wnt/β-catenin and Notch signaling, and that the inhibition of miR-135b is a novel strategy to inhibit tumor metastasis and prevent CSC-induced recurrence in OS.

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MiR-135b promotes proliferation and invasion of osteosarcoma cells via targeting FOXO1

Cited by 53 publications

References 27 publications

Regulatory role of microRNA184 in osteosarcoma cells

Regulatory role of microRNA184 in osteosarcoma cells

Downregulation of lncRNA CASC2 facilitates osteosarcoma growth and invasion through miR‐181a

miR-135b Stimulates Osteosarcoma Recurrence and Lung Metastasis via Notch and Wnt/β-Catenin Signaling

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